化湿降浊法临床运用举隅

笔者在临证时，对外感湿浊之时病，或秽浊着里之杂症，只要湿、浊证存，均用化湿降浊法治疗，每获良效，兹举例如下。１慢性胰腺炎莫某，男，４８岁，１９９７年４月诊。１年前曾因上腹部闷胀作痛，阵发刀割样痛伴恶心呕吐住院。入院诊断为急性胰腺炎，治疗１０余天痊愈。...

重症急性胰腺炎术后死亡原因分析

重症急性胰腺炎(SAP)是一个复杂多变的疾病,病情进展快,并发症多,死亡率高.我院自1990～2000年手术收治17例SAP,其中死亡7例.死亡率41.2%(7/17).笔者就其死亡原因予以浅析.

Therapeutic effects of Caspase-1 inhibitors on acute lung injury in experimental severe acute pancreatitis

AIM： To assess the therapeutic effect of Caspase-1 inhibitors （ICE-I） on acute lung injury （ALI） in experimental severe acute pancreatitis （SAP）. METHODS： Forty-two SD rats were randomly divided into 3 groups： healthy controls （HC, n = 6）; SAP-S group （n = 18）; SAP-ICE-i group （n = 18）. SAP was induced by retrograde infusion of 5% sodium taurocholate into the bile-pancreatic duct. HC rats underwent the same surgical procedures and duct cannulation without sodium taurocholate infusion, in SAP-S group, rats received the first intraperitoneal injection of isotonic saline 2 h after induction of acute pancreatitis and a repeated injection after 12 h. In SAP-ICE-I group, the rats were firstly given ICE inhibitors intraperitoneally 2 h after induction of pancreatitis. As in SAP-S group, the injection was repeated at 12 h. Serum 1L-1β was measured by EUSA. Intrapulmonary expression of Caspase-1, IL-1β and IL-18 mRNA were detected by semi-quantitative RT-PCR. The wet/dry weight ratios and histopathological changes of the lungs were also evaluated. RESULTS： Serum IL-1β levels in SAP-S group were 276.77 ± 44.92 pg/mL at 6 h, 308.99 ± 34.95 pg/mL at 12 h, and 311.60 ± 46.51 pg/mL at 18 h, which were increased significantly （P 〈 0.01, vs HC）. in SAP- ICE-I group, those values were decreased significantly （P 〈 0.01, vs SAP-S）. intrapulmonary expression of Caspase-1, IL-1β and IL-18 mRNA were observed in the HC group, while they were increased significantly in the SAP-S group （P 〈 0.01, vs HC）. The expression of IL-lβ and IL-18 mRNA were decreased significantly in the SAP- ICE-I group （P 〈 0.01, vs SAP-S）, whereas Caspase-1 mRNA expression had no significant difference （P 〉 0.05）. The wet/dry weight ratios of the lungs in the SAP-S group were increased significantly （P 〈 0.05 at 6 h, P 〈 0.01 at 12 h and 18 h, vs HC） and they were decreased significantly in the SAP-ICE-I group （P 〈 0.05, vs SAP-S）.Caspase-1 inhibitors ameliorated the severity of ALl in SAP.CONCLUSION： Caspase-1 activation, and overproduction of IL-1β and IL-18 play an important role in the course of ALI, and Caspase-1 inhibition is effective for the treatment of ALI in experimental SAP.

Protective effects of erythropoietin against acute lung injury in a rat model of acute necrotizing pancreatitis

AIM： TO investigate the effect of exogenous erythro- poietin （EPO） administration on acute lung injury （ALI） in an experimental model of sodium taurodeoxycholate- induced acute necrotizing pancreatitis （ANP）. METHODS： Forty-seven male Wistar albino rats were randomly divided into 7 groups： sham group （n = 5）, 3 ANP groups （n = 7 each） and 3 EPO groups （n = 7 each）. ANP was induced by retrograde infusion of 5% sodium taurodeoxycholate into the common bile duct. Rats in EPO groups received 1000 U/kg intramuscular EPO immediately after induction of ANP. Rats in ANP groups were given 1 mL normal saline instead. All animals were sacrificed at postoperative 24 h, 48 h and 72 h. Serum arnilase, IL-2, IL-6 and lung tissue malondialdehyde （MDA） were measured. Pleural effusion volume and lung/body weight （LW/BW） ratios were calculated. Tissue levels of TNF-a, IL-2 and IL-6 were screened immunohistochemically. Additionally, ox-LDL accumulation was assessed with immune-fluorescent staining. Histopathological alterations in the lungs were also scored.RESULTS： The mean pleural effusion volume, calculated LW/BW ratio, serum IL-6 and lung tissue MDA levels were significantly lower in EPO groups than in ANP groups. No statistically significant difference was observed in either serum or tissue values of IL-2 among the groups. The level of tumor necrosis factor-（~ （TNF-（~） and IL-6 and accumulation of ox-LDL were evident in the lung tissues of ANP groups when compared to EPO groups, particularly at 72 h. Histopathological evaluation confirmed the improvement in lung injury parameters a^er exogenous EPO administration, particularly at 48 h and 72 h. CONCLUSION： EPO administration leads to a significant decrease in ALI parameters by inhibiting polymorphonuclear leukocyte （PMNL） accumulation, decreasing the levels of proinflammatory cytokines in circulation, preserving microvascular endothelial cell integrity and reducing oxidative stress-associated lipid peroxidation and therefore, can be regarded as a cytoprotective agent in ANP-induced ALI.

Proteasome inhibitor ameliorates severe acute pancreatitis and associated lung injury of rats

AIM: To observe the effect of proteasome inhibitor MG-132 on severe acute pancreatitis (SAP) and associated lung injury of rats. METHODS: Male adult SD rats were randomly divided into SAP group, sham-operation group, and MG-132 treatment group. A model of SAP was established by injection of 5% sodium taurocholate into the biliary- pancreatic duct of rats. The MG-132 group was pretreated with 10 mg/kg MG-132 intraperitoneally (ip) 30 min before the induction of pancreatitis. The changes in serum amylase, myeloperoxidase (MPO) activity of pancreatic and pulmonary tissue were measured. The TNF-α level in pancreatic cytosolic fractions was assayed with an enzyme-linked immunosorbent assay (ELISA) kit. Meanwhile, the pathological changes in both pancreatic and pulmonary tissues were also observed. RESULTS: MG-132 significantly decreased serum amylase, pancreatic weight/body ratio, pancreatic TNF-α level, pancreatic and pulmonary MPO activity (P < 0.05). Histopathological examinations revealed that pancreatic and pulmonary samples from rats pretreated with MG-132 demonstrated milder edema, cellular damage, and inflammatory activity (P < 0.05). CONCLUSION: The proteasome inhibitor MG-132 shows a protective effect on severe acute pancreatitis and associated lung injury of rats.

Role of Kupffer cells in acute hemorrhagic necrotizing pancreatitis-associated lung injury of rats

AIM： To investigate the role of Kupffer cells （KCs） in acute hemorrhagic necrotizing pancreatitis-associated lung injury （AHNP-U）. METHODS： Forty-two rats were allocated to four groups [sham operation, AHNP model, gadolinium chloride （GdCl3） pretreatment, GdCl3 control]. In GdCl3 pretreatment group, GdCl3 was administered by caudal vein injection 24 h before the AHNP model induction. Blood from the iliac artery, alveolar macrophages and tissues from the pancreas and lung, were collected in six animals per group 3 and 6 h after acute pancreatitis induction. TNF-α, IL-1 of Lserum, myeloperoxidase （MPO） of lung tissue, NF-κB activation of alveolar macrophages were detected. Serum AST and ALT in sham operation group and GdCl3 control group were tested. In addition, histopathological changes of the pancreas and lung were observed under light microscope. RESULTS： MPO of lung tissue and TNF-α, IL-1 levels of serum were all reduced significantly in GdCl3 pretreatment group compared to those in AHNP group （P〈0.01）. NF-KB activation of alveolar macrophages was also attenuated significantly in GdCl3 pretreatment group compared to that in AHNP group （P〈0.01）. The pathological injury of the lung was ameliorated obviously in GdCl3 pretreatment group compared to that in AHNP group. Nevertheless, the serum amylase level did not reduce and injury of the pancreas was not prevented in GdCl3 pretreatment group. CONCLUSION： Pulmonary injury induced by AHNP is mediated by KC activation and AHNP-LI can be significantly ameliorated by pretreatment with GdCh and KCs play a vital role in AHNP-LI.

Microcirculation disturbance affects rats with acute severe pancreatitis following lung injury

AIM: To study the effects of microcirculation disturbance(MD) on rats with acute severe pancreatitis (ASP).METHODS: We developed ASP rat models, and anatomized separately after 1, 3, 5, 7, and 9 h. We took out blood and did hemorrheologic examination and erythrocyte osmotic fragility test, checked up the water content, capillary permeability, and genetic expression of intercellular adhesion molecule-1 (ICAM-1) in lung tissues, examined the apoptosis degree of blood vessel endothelium while we tested related gene expression of Bax and Bcl-2in lung tissues. We did the same examination in control group.RESULTS: The viscosity of total blood and plasma, the hematocrit, and the erythrocyte osmotic fragility were all increased. Fibrinogen was decreased. The water content in lung tissues and capillary permeability were increased.Apoptosis degree of blood vessel endothelium was increased too. ICAM-1 genetic expression moved up after1 h and reached its peak value after 9 h.CONCLUSION: MD plays an important role in ASP following acute lung injury (ALI). The functional damage of blood vessel endothelium, the apoptosis of capillary vessel endothelium, WBC edging-concentration and the increasing of erythrocyte fragility are the main reasons of ALI.

Pathophysiology of pulmonary complications of acute pancreatitis

Acute pancreatitis in its severe form is complicated by multiple organ system dysfunction, most importantly by pulmonary complications which include hypoxia, acute respiratory distress syndrome, atelectasis, and pleural effusion. The pathogenesis of some of the above complications is attributed to the production of noxious cytokines. Clinically significant is the early onset of pleural effusion, which heralds a poor outcome of acute pancreatitis. The role of circulating trypsin, phospholipase A2, platelet activating factor, release of free fatty acids, chemoattractants such as tumor necrsosis factor （TNF）- alpha, interleukin （IL）-1, IL-6, IL-8, fMet-leu-phe （a bacterial wall product）, nitric oxide, substance P, and macrophage inhlbitor factor is currently studied. The hope is that future management of acute pancreatitis with a better understanding of the pathogenesis of lung injury will be directed against the production of noxious cytokines.

Effect of resveratrol on microcirculation disorder and lung injury following severe acute pancreatitis in rats

AIM: To investigate the mechanism of resveratrol underlying the microcirculation disorder and lung injury following severe acute pancreatitis (SAP). METHODS: Twenty-four rats were divided into 3 groups (SAP, sham and resveratrol groups) randomly. SAP model was established by injecting 4% sodium taurocholate l mL/kg through puncturing pancreatic ducts. Sham (control) group (8 rats) was established by turning over the duodenum. Resveratrol was given at 0.1 mg/kg b.m. intraperitoneally. Rats were sacrificed 9 h after SAP was induced. Blood samples were obtained for hemorrheological examination. Lung tissues were used for pathological observation, and examination of microvascular permeability, dry/wet ratio and myeloperoxidase (MPO) activity. Gene expression of intercellular adhesion molecule-1 (ICAM-1) was detected by RT-PCR. RESULTS: Compared with SAP group, resveratrol relieved the edema and infiltration of leukocytes in the lungs. Resveratrol improved markers of hemorrheology: high VTB (5.77±1.18 mPas vs9.49±1.34 mPas), low VTB (16.12±3.20 mPas vs30.91±7.28 mPas), PV (4.69±1.68 mPas vs 8.00±1.34 mPas), BSR (1.25±0.42 mm/h vs50.03±0.03 mm/h), VPC (54.67±3.08% vs 62.17±3.39%), fibrinogen (203.2?7.8 g/ L vs 51.3±19.1 g/L), original hemolysis (0.45±0.02 vs 0.49±0.02), and complete hemolysis (0.41±0.02 vs 0.43±0.02) (P<0.05). Resveratrol decreased the OD ratio of ICAM-1 gene (0.800±0.03 vs 1.188±0.10), dry/wet ratio (0.74±0.02 vs 0.77±0.03), microvascular permeability (0.079±0.006 vs 0.112±0.004) and MPO activity (4.42±0.32 vs 5.03±0.51) significantly (P<0.05). CONCLUSION: Resveratrol can improve the microcirculation disorder of the lung by decreasing leukocyte-endothelial interaction, reducing blood viscosity, improving the decrease of blood flow, and stabilizing erythrocytes in SAP rats. It may be a potential candidate to treat SAP and its severe complications (ALI).

Pulmonary embolism with acute pancreatitis:A case report and literature review

Acute pancreatitis is an inflammatory disease characterized by local tissue injury which can trigger a systemic inflammatory response.So vascular complications of pancreatitis are a major cause of morbidity and mortality.Pulmonary embolism in acute pancreatitis has been reported to be very rare.We reported a case of pulmonary embolism with acute pancreatitis.A 38-year-old woman broke out upper abdomen pain without definite inducement.She had no nausea and vomiting,fever,dyspnea,cough and expectoration,chest pain.The patient had been diagnosed with acute pancreatitis in local hospital.The patient was treated with antibiotics and proton pump inhibitors,and the abdomen pain was alleviated slightly.But the patient came forth cough and expectoration with a little blood,progressive dyspnea.A computed tomographic scan of the abdomen re-vealed pancreatitis.Subsequent computer tomography angiography of chest revealed pulmonary embolism(both down pulmonary arteries,left pulmonary artery and branch of right pulmonary artery).Dyspnea of the patient got well with thrombolytic treatment and anticoagulation therapy.Pulmonary embolism is a rare but potentially lethal complication of pancreatitis.Familiarity with this complication will aid in its early diagnosis,therapy and prevent pulmonary embolism,a rare but catastrophic phenomenon.

Perforated appendicitis masquerading as acute pancreatitis in a morbidly obese patient

Diagnosis and treatment of common conditions in morbidly obese patients still pose a challenge to physicians and surgeons.Sometimes too much reliance is put on investigations that can lead to a misdiagnosis.This case demonstrates an obese woman admitted under the medical team with a presumed diagnosis of pneumonia, who was later found to have an acute abdomen and raised amylase,which led to an assumed diagnosis of pancreatitis.She died within 24 h of admission and post mortem confirmed the cause of death as systemic sepsis due to perforated appendicitis,with no evidence of pancreatitis.Significantly elevated serum amylase level may occur in non-pancreatitic acute abdomen.

Leptin treatment ameliorates acute lung injury in rats with cerulein-induced acute pancreatitis

AIM:To determine the effect of exogenous leptin on acute lung injury (ALI) in cerulein-induced acute pancreatitis (AP). METHODS:Forty-eight rats were randomly divided into 3 groups. AP was induced by intraperitoneal (i.p.) injection of cerulein (50 μg/kg) four times,at 1 h intervals. The rats received a single i.p. injection of 10 μg/kg leptin (leptin group) or 2 mL saline (AP group) after cerulein injections. In the sham group,animals were given a single i.p. injection of 2 mL saline. Experimental samples were collected for biochemical and histological evaluations at 24 h and 48 h after the induction of AP or saline administration. Blood samples were obtained for the determination of amylase,lipase,tumor necrosis factor (TNF)-a,interleukin (IL)-1β,macrophage inflammatory peptide (MIP)-2 and soluble intercellular adhesion molecule (sICAM)-1 levels,while pancreatic and lung tissues were removed for myeloperoxidase (MPO) activity,nitric oxide (NOx) level,CD40 expression and histological evaluation. RESULTS:Cerulein injection caused severe AP,confirmed by an increase in serum amylase and lipase levels,histopathological findings of severe AP,and pancreatic MPO activity,compared to the values obtained in the sham group. In the leptin group,serum levels of MIP-2,sICMA-1,TNF-a,and IL-1b,pancreatic MPO activity,CD40 expression in pancreas and lung tissues,and NOx level in the lung tissue were lower compared to those in the AP group. Histologically,pancreatic and lungdamage was less severe following leptin administration. CONCLUSION:Exogenous leptin attenuates inflammatory changes,and reduces pro-inflammatory cytokines,nitric oxide levels,and CD40 expression in ceruleininduced AP and may be protective in AP associated ALI.

Diagnosis by endoscopic ultrasound guided fine needle aspiration of tuberculous lymphadenitis involving the peripancreatic lymph nodes: A case report

Pancreatic tuberculosis is an extremely rare form of extrapulmonary disease. The diagnosis preoperatively is difficult because clinical, laboratory and radiologic findings are nonspecific. Published data indicate that these lesions mimic cystic neoplasms of the pancreas and the confirmation of clinical suspicion could only be obtained by an open surgical biopsy. Recently, fine needle aspiration cytology has been shown to be a safe, reliable and cost-effective alternative. We report a new case of a peripancreatic tuberculosis in a 52 year old woman and review the relevant literature, paying special attention to the usefulness of endoscopic ultrasound guided-fine needle aspiration in the diagnosis of abdominal tuberculosis.

Pathogenesis of acute lung injury in severe acute pancreatitis

Objective:To study the pathogenesis of acute lung injury in severe acute pancreatitis (SAP). Methods:Rats were sacrificed at 1, 3, 5, 6, 9 and 12 h after establishment of inducing model. Pancreas and lung tissues were obtained for pathological study, microvascular permeability and MPO examination. Gene expressions of TNF-α and ICAM-1 in pancreas and lung tissues were detected by RT-PCR. Results:After inducing SAP model, the injury degree of the pancreas and the lung increased gradually, accompanied with gradually increased MPO activity and microvascular permeability. Gene expressions of TNF-α and ICAM-1 in pancreas rose at 1 h and reached peak at 7 h. Relatively, their gene expressions in the lungs only rose slightly at 1 h and reached peak at 9-12 h gradually. Conclusion:There is an obvious time window between SAP and lung injury, when earlier protection is beneficial to prevent development of acute lung injury.

A Small Solitary Pulmonary Nodule Discovered by ^(18)F-fluorodeoxyglucose Positron Emission Tomography and CT: Rare Infection Instead of Rare Tumor

THE causes of Cushing＇s syndrome are mainly di- vided into adrenocorticotropic hormone （ACTH） dependent and independent. ACTH dependent hypercortisolism represents excess ACTH se-creting by the pituitary or tumor outside the pituitary; and the latter one is also called as ectopic ACTH syndrome. Thorax is the most common location of causative lesions for ectopic ACTH syndrome, and the size of lesion is too small to be detected in some cases.1＇ 2 Cryptococcal pneumonia usually occurs in immunocompromised patients and excess cortisol production can theoretically produce a state of immunodeficiency. Development of cryptococcal pneumonia concomitant with Cushing syndrome （CS） was rare. Here, we report a case of pulmonary nodule in a patient with CS differentiated with ectopic ACTH-producing tumor. Crypto- coccal pneumonia was diagnosed followinglung resection.

Clodronate-containing liposomes attenuate lung injury in rats with severe acute pancreatitis

Objectives： Severe acute pancreatitis （SAP） can lead to acute lung injury （ALl）. The purpose of this paper is to investigate the protective effect of clodronate-containing liposomes on ALl in rats with SAP. Methods： The thin film method was used to prepare liposomes. Sprague-Dawley rats were randomly divided into three groups. After the SAP model was established by injecting 5% （w/v） sodium taurocholate （2 ml/kg body weight） into the subcapsular space of the pancreata, normal saline was administered to the control （C） group, phosphate buffer solution （PBS）-containing liposome to the P group, and clodronate-containing liposome to the T group through tail veins. Blood samples were obtained from the superior mesenteric vein at 2 and 6 h to measure the levels of amylase, interleukin-6 （IL-6）, and tumor necrosis factor-a （TNF-α）. Morphological changes in the pancreata and lung were observed using hematoxylin and eosin （H＆E） staining, while cell apoptosis was detected using terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling （TUNEL）. In addition, the macrophage marker cluster of differentiation 68 （CD68） in lung tissue was detected with immunohistochemistry. Results： Blood levels of amylase, IL-6, and TNF-α were significantly increased in the P group compared to those in the T group （P〈0.05）. In the T group, large numbers of TUNEL-positive cells were observed, but no or few in the C and P groups. Gross inspection and H＆E staining of pancreata and lung showed dramatic tissue damage, including inflammation and necrosis in the P group. Less remarkable changes were noted in the T group, and the C group exhibited normal histology. The histological scores according to Kaiser＇s criteria were consistent with H＆E findings. The number of CD68-positive macrophages decreased in the T group. Conclusions CIodronate-containing liposomes have a protective effect against ALl in rats with SAP. Blockade of macrophages may represent a novel therapeutic strategy in SAP.

Effect of Chaiqinchengqi decoction on inositol requiring enzyme 1α in alveolar macrophages of dogs with acute necrotising pancreatitis induced by sodium taurocholate

OBJECTIVE: To investigate the effect of Chaiqinchengqi decoction(CQCQD) on inositol requiring enzyme 1α(IRE1α) in alveolar macrophages(AMs)of the dog model of acute necrotising pancreatitis(ANP) induced by sodium taurocholate.METHODS: Fifteen beagle dogs were randomised into a control group,ANP group and CQCQD group(n = 5 per group). ANP was induced by a retrograde duct injection of 50 mg/kg of 5% sodium taurocholate. The dogs in the control group received injections of the same volume of saline as the sodium taurocholate. After the models were induced,the dogs in the CQCQD group were administered 10 m L/kg CQCQD every 2 h for 6 h. Two hours after the last administration of either CQCQD or saline,they were sacrificed by anaesthesia. AMs were collected to determine the IRE1α and Interleukin-1β(IL-1β)m RNA and protein expression,and pancreatic tissues were collected for histopathology analysis.RESULTS: Compared with the ANP group,the m RNA and protein expression of IRE1α and the protein expression of IL-1β of AMs in the CQCQD group were significantly down-regulated,and the pancreatic histopathology score of the CQCQD group also was lower. There was no significant difference in the m RNA expression of IL-1β of AMs between the two groups.CONCLUSION: The CQCQD-induced down-regulation of the IL-1β protein expression may involve the down-regulation of the m RNA and protein expression of IRE1α in AMs.